PHP Code

Using the PHP code extracts allows Academic Staff Profiles to be displayed in a number of different styles including the tabbed format shown below - the data is provided dynamically from the IRIS application, while maintaning the consistent look and feel of your site.

Dr Sally Dawson

  • Telephone:

    020 7679 8935

  • Extension:

    28935

  • Fax:

    020 7679 8990

  • Email:

    sally.dawson@ucl.ac.uk

  • Webpage:

    http://www.ucl.ac.uk/ear

  • Address:

    UCL Ear Institute,
    332 Gray's Inn Rd,
    London,
    WC1X 8EE

  • Appointments:

    Lecturer, The Ear Institute, Faculty of Brain Sciences

Summary

People often ask “Is a disease or condition caused by nature or nurture?” – in fact a lot of the most common diseases are caused by a combination of these two things. I have always been interested in how an individual’s genes and their environment  combine to cause disease and this is one of the things I am studying in hearing loss. I did my PhD in cardiovascular genetics where I learnt about how to study the genetics of complex diseases. When I left I spent some time studying the role a group of genes in the nervous system and by chance one of them turned out to be important in hearing. That’s the kind of thing that can happen in research – you suddenly get taken in a completely new direction.

It was actually quite timely because I was ready to move back into an area of research which was more clinically relevant and was also keen to set up my own group. Here at the UCL Ear Institute it is quite unusual in that there are lots of people working on the same disease but from different points of view which can be very challenging but the building we’re in (Centre for Auditory Research) facilitates interdisciplinary learning by forcing interactions between groups.

This has already proven to be successful –I now have a collaboration with Jonathan Gale’s group and we run some joint research projects together. We’ve also got an interaction with clinicians at the hospital next door which is beneficial for us in terms of getting patient samples and also encouraging clinicians to become more involved in research.

Research Summary

1: Identifying susceptibility of genes for age related hearing loss- looking at how genes differ in people who are prone to hearing loss and understanding the way this increases their risk. Widespread hearing loss is known to be caused by both genetic and environmental factors eventually leading to loss of hair cells in the inner ear. However, it remains unclear why some individuals lose their hearing as they get older while others in the same environment remain undamaged. One explanation is that genetic variation means some individuals are more susceptible to hearing loss caused by environmental damage. We are taking a candidate gene approach to look for common functional changes in genes which may pre-dispose some individuals to hearing loss.
2: Survival mechanisms in hair cells (in collaboration with Jonathan Gale's Group). One of the reasons that the causes of age related hearing loss remain unclear is that we know very little about the molecular pathways of the hair cell. It is loss of the hair cell which is the precipitating cause of hearing loss. The inner ear is frequently subjected to potentially damaging environmental insults such as excessive noise. How the sensory receptor hair cells respond to such stimuli determines whether an insult is pathogenic or is successfully repaired. Deciphering the molecular mechanisms involved in these responses is therefore a pre-requisite to developing interventions to halt or reverse the damage. We have used a subtractive hybridisation strategy to identify a pool of genes whose expression is altered by two hair cell survival factors, Brn-3c and Barhl-1. As part of a collaboration with Dr Jonathan Gale (also at CAR), testing is underway to characterise the role of genes selected from this pool in protecting hair cells from damage and to decipher molecular survival pathways. The aim of our research is to: 1) identify the mechanisms which protect and maintain hair cell function; 2) develop subtractive hybridisation strategy was then used to identify a pool of genes whose strategies to improve the survival of hair cells; 3) test the efficacy of these in protecting against damage.
3. Investigating the Causes of Otosclerosis. Otosclerosis is a common form of hearing loss caused by dysregulation of the stapes bone in the middle ear. In a joint project with Prof Shak Saeed, surgeon at the Royal Nose, Throat and Ear Hospital we are examining the cause of the dysregulation in stapes bone removed from patients and performing a genetic analysis to identify the underlying cause of this disorder.


Keywords: Ageing, Genetics, Gene expression, Hearing, Hearing and balance


Conditions: Auditory system disorders, Deafness


Methods: Gene expression profiling - single cell , Gene expression profiling - tissue level, Genetically encoded reporters/indicators, Genetic screens, Genomic analyses

Research Activities

  • Ageing
  • Cellular Mechanisms of Hearing
  • Deafness genetics
  • Genetic deafness
  • Genetics of hearing
  • Identifying susceptibility of genes for age related hearing loss. Investigating survival mechanisms
  • Intracellular and intercellular signalling mechanisms in health and disease
  • Noise-induced hearing loss
  • Otosclerosis
  • Speech and Hearing Science
  • Stress Granules
  • ageing

Recent Publications

Displaying 50 most recent publications. For the full list please visit UCL Discovery

  1. Nolan LS,Maier H,Hermans-Borgmeyer I,Girotto G,Ecob R,Pirastu N,Cadge BA,Hubner C,Gasparini P,Strachan DP,Davis A,Dawson SJ (2013) Estrogen-related receptor gamma and hearing function: evidence of a role in humans and mice. Neurobiology of Aging.
  2. Nolana LS,Maierb H,Hermans-Borgmeyerc I,Girottod G,Ecoba R,Pirastud N,Cadgea BA,Hübnere C,Gasparinid P,Strachanf DP,Davisa A,Dawson SJ (2013) ESRRG and hearing function; evidence of a role in humans and mice Neurobiology of Aging.
  3. Nolan LS,Cadge BA,Gomez-Dorado M,Dawson SJ (2013) A functional and genetic analysis of SOD2 promoter variants and their contribution to age-related hearing loss. Mech Ageing Dev. 10.1016/j.mad.2013.02.009.
  4. Dawson SJ (2012) The genetics of ototoxicity ENT and Audiology News, 21(1), 70 - 73.
  5. Al-Malky G,Suri R,Dawson SJ,Sirimanna T,Kemp D (2011) Aminoglycoside antibiotics cochleotoxicity in paediatric cystic fibrosis (CF) patients: A study using extended high-frequency audiometry and distortion product otoacoustic emissions. Int J Audiol, 50(2), 112 - 122. 10.3109/14992027.2010.524253.
  6. Towers ER,Kelly JJ,Sud R,Gale JE,Dawson SJ (2011) Caprin-1 is a target of the deafness gene Pou4f3 and is recruited to stress granules in cochlear hair cells in response to ototoxic damage Journal of Cell Science, 124(6).
  7. DAWSON S (2010) The Role of Genetics in Age-Related Hearing Loss ENT & Audiology News, 19(4), 100 - 102.
  8. Nolan LS,Jagutpal SS,Cadge BA,Woo P,Dawson SJ (2007) Identification and functional analysis of common sequence variants in the DFNA15 gene, Brn-3c GENE, 400(1-2), 89 - 97. 10.1016/j.gene.2007.05.023.
  9. Sud R,Jones CM,Banfi S,Dawson SJ (2005) Transcriptional regulation by Barh11 and Brn-3c in organ of corti derived cell lines MOL BRAIN RES, 141(2), 174 - 180. 10.1016/j.molbrainres.2005.09.007.
  10. Sud R,Jones CM,Banfi S,Dawson SJ (2005) Transcriptional regulation by Barhl1 and Brn-3c in organ of corti derived cell lines Molecular Brain Research, 141(2), 174 - 180.
  11. Clough RL,Sud R,Davis-Silberman N,Hertzano R,Avraham KB,Holley M,Dawson SJ (2004) Brn-3c (POU4F3) regulates BDNF and NT-3 promoter activity BIOCHEM BIOPH RES CO, 324(1), 372 - 381. 10.1016/j.bbrc.2004.09.074.
  12. Weiss S,Gottfried I,Mayrose I,Khare SL,Xiang MQ,Dawson SJ,Avraham KB (2003) The DFNA15 deafness mutation affects POU4F3 protein stability, localization, and transcriptional activity MOL CELL BIOL, 23(22), 7957 - 7964. 10.1128/MCB.23.22.7957-7964.2003.
  13. Lindahl GE,Chambers RC,Papakrivopoulou J,Dawson SJ,Jacobsen MC,Bishop JE,Laurent GJ (2002) Activation of fibroblast procollagen alpha 1(I) transcription by mechanical strain is transforming growth factor-beta-dependent and involves increased binding of CCAAT-binding factor (CBF/NF-Y) at the proximal promoter J BIOL CHEM, 277(8), 6153 - 6161. 10.1074/jbc.M108966200.
  14. Avraham KB,Khare SL,Xiang M,Dawson SJ,Weiss S (2000) The biological basis for autosomal dominant nonsyndromic hearing loss DFNA15: expression, DNA binding and transcription properties..
  15. Dawson SJ,Palmer RD,Morris PJ,Latchman DS (1998) Functional role of position 22 in the homeodomain of Brn-3 transcription factors NEUROREPORT, 9(10), 2305 - 2309.
  16. Liu YZ,Lee IK,Locke I,Dawson SJ,Latchman DS (1998) Adjacent proline residues in the inhibitory domain of the Oct-2 transcription factor play distinct functional roles NUCLEIC ACIDS RES, 26(10), 2464 - 2472.
  17. Gay RD,Dawson SJ,Murphy WJ,Russell SW,Latchman DS (1998) Activation of the iNOS gene promoter by Brn-3 POU family transcription factors is dependent upon the octamer motif in the promoter BBA-GENE STRUCT EXPR, 1443(3), 315 - 322.
  18. Smith MD,Dawson SJ,Boxer LM,Latchman DS (1998) The N-terminal domain unique to the long form of the Brn-3a transcription factor is essential to protect neuronal cells from apoptosis and for the activation of Bcl-2 gene expression NUCLEIC ACIDS RES, 26(18), 4100 - 4107.
  19. Smith MD,Dawson SJ,Latchman DS (1997) The Brn-3a transcription factor induces neuronal process outgrowth and the coordinate expression of genes encoding synaptic proteins MOL CELL BIOL, 17(1), 345 - 354.
  20. Smith MD,Morris PJ,Dawson SJ,Schwartz ML,Schlaepfer WW,Latchman DS (1997) Coordinate induction of the three neurofilament genes by the Brn-3a transcription factor J BIOL CHEM, 272(34), 21325 - 21333.
  21. Smith MD,Dawson SJ,Latchman DS (1997) Inhibition of neuronal process outgrowth and neuronal specific gene activation by the Brn-3b transcription factor J BIOL CHEM, 272(2), 1382 - 1388.
  22. Morris PJ,Dawson SJ,Wilson MC,Latchman DS (1997) A single residue within the homeodomain of the Brn-3 POU family transcription factors determines whether they activate or repress the SNAP-25 promoter NEUROREPORT, 8(8), 2041 - 2045.
  23. Deans ZC,Dawson SJ,Kilimann MW,Wallace D,Wilson MC,Latchman DS (1997) Differential regulation of genes encoding synaptic proteins by the Oct-2 transcription factor MOL BRAIN RES, 51(1-2), 1 - 7.
  24. Gay RD,Dawson SJ,Latchman DS (1997) The different inhibitory domains of the Oct-2 transcription factor have distinct functional activities FEBS LETT, 416(2), 135 - 138.
  25. Liu YZ,Dawson SJ,Latchman DS (1996) Alternative splicing of the Brn-3a and Brn-3b transcription factor RNAs is regulated in neuronal cells J MOL NEUROSCI, 7(1), 77 - 85.
  26. Dawson SJ,Liu YZ,Rodel B,Moroy T,Latchman DS (1996) The ability of POU family transcription factors to activate or repress gene expression is dependent on the spacing and context of their specific response elements BIOCHEM J, 314, 439 - 443.
  27. BudhramMahadeo V,Morris PJ,Lakin ND,Dawson SJ,Latchman DS (1996) The different activities of the two activation domains of the Brn-3a transcription factor are dependent on the context of the binding site J BIOL CHEM, 271(15), 9108 - 9113.
  28. Morris PJ,Lakin ND,Dawson SJ,Ryabinin AE,Kilimann MW,Wilson MC,Latchman DS (1996) Differential regulation of genes encoding synaptic proteins by members of the Brn-3 subfamily of POU transcription factors MOL BRAIN RES, 43(1-2), 279 - 285.
  29. Deans Z,Dawson SJ,Xie JL,Young AP,Wallace D,Latchman DS (1996) Differential regulation of the two neuronal nitric-oxide synthase gene promoters by the Oct-2 transcription factor J BIOL CHEM, 271(50), 32153 - 32158.
  30. Liu YZ,Dawson SJ,Gerster T,Friedl E,Pengue G,Matthias P,Lania L,Latchman DS (1996) The ability of the inhibitory domain of the POU family transcription factor Oct-2 to interfere with promoter activation by different classes of activation domains is dependent upon the nature of the basal promoter elements J BIOL CHEM, 271(34), 20853 - 20860.
  31. Dawson SJ,Morris PJ,Latchman DS (1996) A single amino acid change converts an inhibitory transcription factor into an activator J BIOL CHEM, 271(20), 11631 - 11633.
  32. GREEN FR,LANE A,THOMAS AE,DAWSON S,MILLER G,HAMSTEN A,HUMPHRIES SE (1995) GENE ENVIRONMENT INTERACTIONS AND THE RISK OF THROMBOSIS ATHEROSCLEROSIS X, 1066, 805 - 807.
  33. Ye S,Green FR,Scarabin PY,Nicaud V,Bara L,Dawson SJ,Humphries SE,Evans A,Luc G,Cambou JP (1995) The 4G/5G genetic polymorphism in the promoter of the plasminogen activator inhibitor-1 (PAI-1) gene is associated with differences in plasma PAI-1 activity but not with risk of myocardial infarction in the ECTIM study. Etude CasTemoins de I'nfarctus du Mycocarde. Thromb Haemost, 74(3), 837 - 841.
  34. YE S,GREEN FR,SCARABIN PY,NICAUD V,BARA L,DAWSON SJ,HUMPHRIES SE,EVANS A,LUC G,CAMBOU JP,ARVEILER D,HENNEY AM,CAMBIEN F (1995) THE 4G/5G GENETIC-POLYMORPHISM IN THE PROMOTER OF THE PLASMINOGEN-ACTIVATOR INHIBITOR-1 (PAI-1) GENE IS ASSOCIATED WITH DIFFERENCES IN PLASMA PAI-1 ACTIVITY BUT NOT WITH RISK OF MYOCARDIAL-INFARCTION IN THE ECTIM STUDY THROMB HAEMOSTASIS, 74(3), 837 - 841.
  35. Deans L,Dawson SJ,Buttery L,Polak JM,Wallace D,Latchman DS (1995) Direct evidence that the POU family transcription factor Oct-2 represses the cellular tyrosine hydroxylase gene in neuronal cells J MOL NEUROSCI, 6(3), 159 - 167.
  36. LILLYCROP KA,DAWSON SJ,ESTRIDGE JK,GERSTER T,MATTHIAS P,LATCHMAN DS (1994) REPRESSION OF A HERPES-SIMPLEX VIRUS IMMEDIATE-EARLY PROMOTER BY THE OCT-2 TRANSCRIPTION FACTOR IS DEPENDENT ON AN INHIBITORY REGION AT THE N-TERMINUS OF THE PROTEIN MOL CELL BIOL, 14(11), 7633 - 7642.
  37. DAWSON SJ,YOON SO,CHIKARAISHI DM,LILLYCROP KA,LATCHMAN DS (1994) THE OCT-2 TRANSCRIPTION FACTOR REPRESSES TYROSINE-HYDROXYLASE EXPRESSION VIA A HEPTAMER TAATGARAT-LIKE MOTIF IN THE GENE PROMOTER NUCLEIC ACIDS RES, 22(6), 1023 - 1028.
  38. DAWSON SJ,WIMAN B,HAMSTEN A,GREEN F,HUMPHRIES S,HENNEY AM (1993) THE 2 ALLELE SEQUENCES OF A COMMON POLYMORPHISM IN THE PROMOTER OF THE PLASMINOGEN-ACTIVATOR INHIBITOR-1 (PAI-1) GENE RESPOND DIFFERENTLY TO INTERLEUKIN-1 IN HEPG2 CELLS J BIOL CHEM, 268(15), 10739 - 10745.
  39. DAWSON S,HENNEY A (1992) THE STATUS OF PAI-1 AS A RISK FACTOR FOR ARTERIAL AND THROMBOTIC DISEASE - A REVIEW ATHEROSCLEROSIS, 95(2-3), 105 - 117.
  40. THOMAS AE,GREEN FR,DAWSON SJ,LANE A,HENNEY AM,KELLEHER CH,WILKES HC,BRENNAN PJ,CRUICKSHANK JK,HAMSTEN A,WIMAN B,MEADE TW,HUMPHRIES SE (1992) POSSIBILITIES OF DNA ANALYSIS FOR THE DETECTION OF PREDISPOSITION TO THROMBOTIC DISEASE PLASMINOGEN ACTIVATION IN FIBRINOLYSIS, IN TISSUE REMODELING, AND IN DEVELOPMENT, 667, 332 - 342.
  41. THOMAS AE,GREEN FR,DAWSON SJ,LANE A,HENNEY AM,KELLEHER CH,WILKES HC,BRENNAN PJ,CRUICKSHANK JK,HAMSTEN A,WIMAN B,MEADE TW,HUMPHRIES SE (1992) POSSIBILITIES OF DNA ANALYSIS FOR THE DETECTION OF PREDISPOSITION TO THROMBOTIC DISEASE ANN NY ACAD SCI, 667, 332 - 342.
  42. HUMPHRIES SE,LANE A,DAWSON S,GREEN FR (1992) THE STUDY OF GENE-ENVIRONMENT INTERACTIONS THAT INFLUENCE THROMBOSIS AND FIBRINOLYSIS - GENETIC-VARIATION AT THE LOCI FOR FACTOR-VII AND PLASMINOGEN-ACTIVATOR INHIBITOR-1 ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE, 116(12), 1322 - 1329.
  43. Humphries SE,Green FR,Temple A,Dawson S,Henney A,Kelleher CH,Wilkes H,Meade TW,Wiman B,Hamsten A (1992) Genetic factors determining thrombosis and fibrinolysis. Ann Epidemiol, 2(4), 371 - 385.
  44. HUMPHRIES SE,GREEN F,DAWSON S,HAMSTEN A (1991) INTERACTION BETWEEN GENOTYPE AND ENVIRONMENTAL-FACTORS IN THE DEVELOPMENT OF ATHEROSCLEROTIC-THROMBOTIC ARTERIAL DISEASES THROMB HAEMOSTASIS, 65(6), 816 - 816.
  45. DAWSON SJ,WIMAN B,HAMSTEN A,GREEN F,HENNEY AM,HUMPHRIES S (1991) A COMMON POLYMORPHISM IN THE PLASMINOGEN-ACTIVATOR INHIBITOR-1 (PAI-1) PROMOTER SHOWS ALLELE SPECIFIC DIFFERENTIAL BINDING TO HEPG2 NUCLEAR EXTRACTS AND IS ASSOCIATED WITH ALTERED PLASMA PAI-1 LEVELS AM J HUM GENET, 49(4), 426 - 426.
  46. DAWSON SJ,WIMAN B,HAMSTEN A,GREEN F,HENNEY AM,HUMPHRIES S (1991) ALLELE SPECIFIC DIFFERENTIAL BINDING OF HEPG2 NUCLEAR EXTRACTS TO A COMMON POLYMORPHISM IN THE PLASMINOGEN-ACTIVATOR INHIBITOR-1 (PAI-1) PROMOTER WHICH IS ASSOCIATED WITH ALTERED PLASMA PAI-1 LEVELS THROMB HAEMOSTASIS, 65(6), 806 - 806.
  47. DAWSON S,HAMSTEN A,WIMAN B,HENNEY A,HUMPHRIES S (1991) GENETIC-VARIATION AT THE PLASMINOGEN-ACTIVATOR INHIBITOR-1 LOCUS IS ASSOCIATED WITH ALTERED LEVELS OF PLASMA PLASMINOGEN-ACTIVATOR INHIBITOR-1 ACTIVITY ARTERIOSCLER THROMB, 11(1), 183 - 190.
  48. HENNEY AM,GREEN FR,DAWSON SJ,YE S,LANE A,HUMPHRIES SE,SCARABIN PY,CAMBIEN F,EVANS A,CAMBOU JP,ARVEILER D,BARA L (1991) PAI-1 AND FACTOR-VII GENE POLYMORPHISMS AND ASSOCIATION WITH PLASMA-LEVELS IN THE ECTIM STUDY, A MULTICENTER, CASE-CONTROL STUDY OF MYOCARDIAL-INFARCTION THROMB HAEMOSTASIS, 65(6), 993 - 993.
  49. DAWSON SJ,HENNEY AM,HUMPHRIES S,HAMSTEN A (1990) USE OF PCR TO GENOTYPE A POLYMORPHIC DINUCLEOTIDE REPEAT WITHIN THE PAI-1 GENE IN PATIENTS WITH A RECENT MI J MED GENET, 27(3), 207 - 207.
  50. DAWSON S,HAMSTEN A,WIMAN B,HENNEY A,HUMPHRIES S (1990) GENETIC-VARIATION AT THE PLASMINOGEN-ACTIVATOR INHIBITOR-1 (PAI-1) LOCUS FIBRINOLYSIS, 4, 51 - 53.

Biography

People often ask “Is a disease or condition caused by nature or nurture?” – in fact a lot of the most common diseases are caused by a combination of these two things. I have always been interested in how an individual’s genes and their environment  combine to cause disease and this is one of the things I am studying in hearing loss. I did my PhD in cardiovascular genetics where I learnt about how to study the genetics of complex diseases. When I left I spent some time studying the role a group of genes in the nervous system and by chance one of them turned out to be important in hearing. That’s the kind of thing that can happen in research – you suddenly get taken in a completely new direction.

It was actually quite timely because I was ready to move back into an area of research which was more clinically relevant and was also keen to set up my own group. Here at the UCL Ear Institute it is quite unusual in that there are lots of people working on the same disease but from different points of view which can be very challenging but the building we’re in (Centre for Auditory Research) facilitates interdisciplinary learning by forcing interactions between groups.

This has already proven to be successful –I now have a collaboration with Jonathan Gale’s group and we run some joint research projects together. We’ve also got an interaction with clinicians at the hospital next door which is beneficial for us in terms of getting patient samples and also encouraging clinicians to become more involved in research.

Qualifications

  • 1992: Doctor of Philosophy, University of London
  • 1985: Bachelor of Science (Honours), University of East Anglia

Keywords

  • Ageing
  • Analysing the causes of adult onset hearing loss
  • Auditory system disorders
  • Deafness
  • Gene expression
  • Gene expression profiling - single cell
  • Gene expression profiling - tissue level
  • Genetic screens
  • Genetically encoded reporters/indicators
  • Genetics
  • Genomic analyses
  • Hearing
  • Hearing and balance
  • Otosclerosis
  • Stress Granules